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Related Experiment Video

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Maternal Benzophenone Exposure Impairs Hippocampus Development and Cognitive Function in Mouse Offspring.

Fengzhen Cui1, Qingfei Pan2, Siyi Wang3

  • 1Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|October 29, 2021
PubMed
Summary

Prenatal exposure to 4-hydroxybenzophenone (4HBP), a benzophenone metabolite, harms hippocampus development and causes cognitive issues in mice. This highlights the neurodevelopmental toxicity of BP, urging caution during pregnancy.

Keywords:
4-hydroxybenzophenoneendoplasmic reticulum stressneurodevelopmental toxicityp65protein kinase R-like ER kinase-eIF2α

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Area of Science:

  • Neuroscience
  • Toxicology
  • Developmental Biology

Background:

  • Benzophenones are common in personal care products, but their neurodevelopmental toxicity is poorly understood.
  • Previous studies suggest a link between maternal exposure to 4-hydroxybenzophenone (4HBP) and impaired child neurodevelopment.

Purpose of the Study:

  • To investigate the causal relationship and mechanisms of 4HBP neurodevelopmental toxicity.
  • To determine the impact of prenatal versus postnatal 4HBP exposure on offspring neurodevelopment.

Main Methods:

  • Exposure of mice to environmentally relevant levels of 4HBP during prenatal or postnatal periods.
  • Assessment of hippocampus development and cognitive function in offspring.
  • Transcriptomic analysis of hippocampal neural stem cells.
  • Investigation of the PERK and NFκB signaling pathways.
  • Validation in a human brain organoid model.

Main Results:

  • Prenatal 4HBP exposure, but not postnatal, impaired hippocampus development and caused cognitive dysfunction in mice.
  • 4HBP induced endoplasmic reticulum stress, apoptosis, and inflammation in neural stem cells via the PERK pathway.
  • Inhibition of the PERK pathway mitigated 4HBP-induced neurodevelopmental abnormalities in mice and human brain organoids.

Conclusions:

  • Prenatal exposure to 4HBP poses a significant risk for neurodevelopmental toxicity.
  • The PERK signaling pathway is a key mediator of 4HBP-induced neurotoxicity.
  • These findings underscore the need for caution regarding benzophenone exposure during pregnancy.